Transient triiodothyronine deficiency. Absence of effect on basal or adrenaline-stimulated carbohydrate and lipid metabolism in man

Abstract

Severe stress is accompanied by a fall in circulating triiodothyronine levels as well as increases in secretion of several hormones including adrenaline. The present study was designed to test the hypothesis that the fall in triiodothyronine may counteract in part the catabolic effects of stress hormones such as adrenaline. Transient hypothyroidism was induced by administration orally of sodium ipodate (3 g). Adrenaline infusions (6 micrograms/min for 2 hours) were performed in five healthy men before and four days after ipodate was given. Circulating triiodothyronine levels decreased from 1.7 +/- 0.1 to 1.1 +/- 0.1 nmol/l (p less than 0.001), associated with a small rise in serum thyroxine, but basal circulating concentrations of glucose, the gluconeogenic precursors, NEFA and 3-hydroxybutyrate were unaltered. Circulating insulin, glucagon and growth hormone concentrations were also similar with and without prior ipodate ingestion. Adrenaline infusion produced a rise in blood glucose (4.9 +/- 0.2 to 8.5 +/- 0.4 mmol/l at 60 min), lactate, pyruvate and the lactate: pyruvate ratio, which was unaltered by ipodate. Blood glycerol (0.04 +/- 0.004 to 0.13 +/- 0.03 mmol/l at 30 min), plasma NEFA (0.52 +/- 0.05 to 1.31 +/- 0.17 mmol/l at 30 min) and blood 3-hydroxybutyrate concentrations (0.04 +/- 0.004 to 0.26 +/- 0.07 mmol/l at 50 min) were elevated by adrenaline, with similar responses obtained after ipodate. Ipodate also did not influence the circulating insulin and glucagon response to adrenaline infusion. A transient decrease in circulating triiodothyronine concentrations induced by ipodate does not modulate the hormonal and metabolic response to adrenaline in normal man.